Proteinuria - Causes and Symptoms

Definition

Proteinuria means the presence of amounts greater than 150 mg / day of protein in the urine.

The causes can be classified according to the onset mechanism. In most cases, proteinuria is the consequence of glomerulopathies, which generally manifest as nephrotic syndrome. The latter is characterized by a clinical picture of severe proteinuria (> 3.5 g / day) with edema, hypoalbuminemia, hyperlipidemia and lipiduria. Nephrotic syndrome may represent a primary process (glomerulonephritis) or secondary to a systemic condition (eg diabetic nephropathy, pre-eclampsia, infections, lupus nephritis and amyloidosis).

The high concentration of proteins determines the production of more or less dense foamy urines. Proteinuria is present in many kidney disorders and is associated with other urinary abnormalities (eg hematuria). The isolated form manifests itself without other symptoms.

Functional proteinuria

Functional proteinuria is a temporary increase in protein excretion in the urine, caused by glomerular hemodynamic changes. In particular, the increase in protein in the urine occurs when the increase in renal blood flow pours more of them into the nephron. This can result from intense physical activity, fever, dehydration and emotional stress. Functional proteinuria is reversed when renal blood flow returns to normal.

Orthostatic proteinuria

A particular type of functional, relatively common proteinuria is called orthostatic or postural. This is a benign condition, typically seen in subjects under the age of 30 with preserved kidney function. In this context, proteinuria is moderate and occurs mainly when the patient is in an upright position (protein excretion of less than 2 g per day), while it is absent after a period of bed rest, such as after night rest. Thus, urine typically contains more protein during waking hours. Generally, orthostatic proteinuria follows, like functional protein, a benign course, often with spontaneous resolution.

Glomerular proteinuria

Glomerular proteinuria derives from diseases of the renal glomerulus, which usually imply an increase in permeability at this level; this allows a greater quantity of plasma proteins to pass into the filtrate. Proteinuria may result from primitive glomerular disorders, such as membranous nephropathy, glomerulonephritis with minimal injury, and focal segmental glomerulosclerosis.

Important secondary causes include diabetes mellitus, use of certain drugs (including NSAIDs and antibiotics), infections (HIV, hepatitis B and C, post-streptococcal disease, syphilis, malaria and endocarditis), infiltrative processes (such as amyloidosis) and pre-eclampsia. Glomerular proteinuria can also derive from diseases with an autoimmune etiology (such as lupus nephritis) and malignant neoplasms (eg carcinoma of the colon, stomach or lung and lymphoma).

Tubular proteinuria

Tubular proteinuria results from renal tubulo-interstitial abnormalities that prevent protein reabsorption by the proximal tubule.

Causative factors are often accompanied by other defects of tubular function (eg loss of bicarbonate and glycosuria) and sometimes by glomerulopathies.

Tubular proteinuria can be found in the presence of Fanconi syndrome, acute tubular necrosis, tubulointerstitial nephritis and polycystic kidney disease.

Hyperafflora proteinuria

Hyperafflower proteinuria occurs when an excessive amount of small plasma proteins (eg light chains of immunoglobulins produced in multiple myeloma) exceeds the capacity of reabsorption of the proximal tubules. Possible causes include acute monocytic leukemia and myelodysplastic syndromes.